Evidence map›Paper›PMID 24496952›Full record

ArticleStem cells (Dayton, Ohio)2014

Switch from canonical to noncanonical Wnt signaling mediates high glucose-induced adipogenesis.

Emily C Keats, James M Dominguez, Maria B Grant, Zia A Khan

Open access · bronzeAbstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
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  14. The role of wnt signaling in diabetes-induced osteoporosis.Diabetology & metabolic syndrome · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Noncanonical Wnt Signaling Promotes Myofibroblast Differentiation in Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2021
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Emily C KeatsDepartment of Pathology, Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.
James M Dominguez
Maria B Grant
Zia A Khan
University of Florida · USLawson Health Research Institute · CAWestern University · CA

Funding

NITRIC OXIDE IN THE PATHOGENESIS OF DIABETIC RETINOPATHYR01EY012601 · NEI · UNIVERSITY OF FLORIDA · PI Julia V Busik, Maria Bartolomeo Grant · 1998 to 2026
$9.6M
Targeting the IGF-1 System in Retinal AngiogenesisR01EY007739 · NEI · UNIVERSITY OF FLORIDA · PI ABCOUWER, STEVEN F, GRANT, MARIA BARTOLOMEO · 1995 to 2015
$5.4M
Vascular Reparative Mechanism by ACE2/Ang-(1-7)in DiabetesR01HL110170 · NHLBI · UNIVERSITY OF FLORIDA · PI GRANT, MARIA BARTOLOMEO · 2011 to 2015
$2.2M
NO Dysregulation of the Peripheral Clock in Diabetic ComplicationsR01DK090730 · NIDDK · UNIVERSITY OF FLORIDA · PI GRANT, MARIA BARTOLOMEO · 2010 to 2013
$1.3M
HORMONES &NEOVASCULARIZATION IN DIABETIC RETINOPATHYR29EY007739 · NEI · UNIVERSITY OF FLORIDA · PI GRANT, MARIA B · 1989 to 1993
–
NEI NIH HHS EY007739NEI NIH HHS EY012601NEI NIH HHS R01 EY007739NEI NIH HHS R01 EY012601NHLBI NIH HHS R01 HL110170NIDDK NIH HHS DK090730NIDDK NIH HHS R01 DK090730
6 · The paper itself

Abstract

Human bone marrow mesenchymal progenitor cells (MPCs) are multipotent cells that play an essential role in endogenous repair and the maintenance of the stem cell niche. We have recently shown that high levels of glucose, conditions mimicking diabetes, cause impairment of MPCs, resulting in enhanced adipogenesis and suppression of osteogenesis. This implies that diabetes may lead to reduced endogenous repair mechanisms through altering the differentiation potential of MPCs and, consequently, disrupting the stem cell niche. Phenotypic alterations in the bone marrow of long-term diabetic patients closely resemble this observation. Here, we show that high levels of glucose selectively enhance autogenous Wnt11 expression in MPCs to stimulate adipogenesis through the Wnt/protein kinase C noncanonical pathway. This novel mechanism may account for increased bone marrow adipogenesis, severe bone loss, and reduced vascular stem cells leading to chronic secondary complications of diabetes.

Indexed as

AC133 AntigenAdipogenesisAgedAngiopoietin-2AnimalsAntigens, CDbeta CateninBone MarrowCell DifferentiationDiabetes Mellitus, ExperimentalGlucoseGlycoproteinsHumansMesenchymal Stem CellsMiddle AgedModels, BiologicalAC133 AntigenAngiopoietin-2Antigens, CDbeta CateninGlucoseGlycoproteinsPeptidesProtein Kinase CSmall Molecule LibrariesWnt11 protein, humanWnt ProteinsAdipogenesisCell-autogenous regulationDiabetesNoncanonical signalingProtein kinase CWnt signaling

Identifiers

PMID24496952
PMCPMC4037346
OpenAlexW1550732900

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.